In patients with chronic obstructive pulmonary disease (COPD), subclinical left ventricular (LV) systolic dysfunction is likely to be detected when measured by tissue Doppler imaging (TDI), even in patients without pulmonary hypertension (PH), according to study results published in PLoS ONE.

TDI is a sensitive tool for detecting subclinical LV dysfunction. Therefore, researchers aimed to characterize LV dysfunction and investigate the prevalence of subclinical LV dysfunction with these novel imaging techniques in patients with stable COPD both with and without PH, and without known LV disease.

The study included 100 outpatients with COPD and 34 control individuals. Patients were divided by invasive mean pulmonary artery pressure (mPAP) in COPD-PH (≥25 mm Hg) and COPD-non-PH (<25 mm Hg); the patients with mPAP <25 mm Hg were subdivided into mPAP ≤20 mm Hg and 21 to24 mm Hg. LV myocardial performance index (MPI) ≥0.51 and strain ≤-15.8% were considered abnormal.

LV MPI ≥0.51 was found in 64.9% and 88.5%, and LV strain ≤-15.8% in 62.2% and 76.9% in patients with COPD-non-PH and COPD-PH, respectively. LV MPI and LV strain were also impaired in patients with mPAP<20 mm Hg. Residual volume and stroke volume were most associated with LV MPI and LV strain, respectively, in multiple regression analyses.


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LV diastolic function was assessed by the ratio between peak early (E) and late (A) velocity, early TDI E’, E/E’, isovolumic relaxation time, and left atrium volume. Researchers found that except for isovolumic relaxation time, standard diastolic echo indices E/A, E’, E/E’ and left atrium volume did not change from normal individuals (ie, those with normal PAP) to COPD-non-PH.

“Subclinical LV systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure,” the researchers wrote. “Evidence of LV diastolic dysfunction was hardly present as measured by conventional echo indices.”

Reference

Hilde JM, Hisdal J, Skjørten I, et al. Left ventricular dysfunction in COPD without pulmonary hypertension. PLoS ONE. 2020;15(7):e0235075.